The aim of this study is to elucidate the role of both the epithelial and connective tissue mast cell in the etiology and/or pathogenesis of selected human gingival and periodontal lesions, with particular emphasis on the sulcular lesion of chronic periodontal disease. The fine structure of mast cells associated with these lesions will be studied in human biopsies, using a technique which reliably preserves cytologic features including mast cell granules. Normal gingival specimens will provide baseline data. Information will be obtained regarding the distribution and morphology of mast cells; their cytologic features, including the presence and relative amounts of organelles involved in granule synthesis; signs of granule release; and the relationship of mast cells to other cell types and to regions of tissue damage. Staining of certain specimens with ruthenium red will allow for an accurate evaluation of mast cell degranulation. Special attention will be given to the intraepithelial mast cell. Interpretation of micrographs obtained will provide indirect information concerning mast cell function and activity in the specimens. More direct evidence regarding mast cell function will then be obtained by means of in vitro experiments using gingival explants. A system will be established for the study of mast cell degranulation in gingiva in vitro which can then be used to assess the effect of various substances, e.g., bacterial antigens. In addition, the possibility of gingival mast cells having a phagocytic role will be investigated in vitro by means of electron microscopy using an electron-opaque market. BIBLIOGRAPHIC REFERENCES: Barnett, M. L.: The non-keratinocyte intraepithelial cell population in lichen planus. An ultrastructural characterization of cells in gingival lesions. Oral Surg. 41: 338-353, 1976. Barnett, M. L., Sun, S., Binder, W. and Beutner, E. H.: Ultrastructural study of pemphigus lesions produced in vitro. International Association for Dental Research. Program and Abstracts, February, 1976, No. 200.